Acute lymphoblastic leukemia (ALL) is a form of leukemia that is characterized by the presence of excess lymphoblasts due to the continuous multiplication of malignant immature white blood cells. ALL is a disease that rapidly progresses and is characterized by crowding of normal cells in the bone marrow due to the continuous multiplication of immature white blood cells.
Precursor T-cell acute lymphoblastic leukemia (T-ALL) causes 15% of acute leukemias in childhood, and approximately 40% of lymphomas in childhood. Acute refers to the relatively short time course of the disease, as it can be fatal in as little as a few weeks if left untreated. Most common in adolescent males, T-ALL's morphology is identical to that of precursor B-cell lymphoblastic leukemia. The rapid progression or relatively short time course of T-ALL without treatment makes early diagnosis extremely important since early intervention may delay onset of the disease and ultimately increase survival rates.
Currently no cellular markers specific for acute T-ALL are known, making diagnosis of the disease difficult. The only effective diagnostic method for acute T-ALL includes medical history, physical examination, complete blood count, and blood smears. There is an unmet need for the identification of cellular markers specific for acute T-ALL. The development of a diagnostic cellular marker that could aid in the diagnosis and treatment of T-ALL in its early stages is desirable.
Acute myeloid leukemia (AML) is one of the most common types of leukemia in adults (50), (51). Despite major advances in our understanding of the biology of AML, the 5-year survival of AML patients is only 20-40%. It has been proposed that AML originates from self-renewing hematopoietic stem cells (HSC)/progenitors that have acquired multiple genetic and/or epigenetic changes (52). These cells initiate a developmental hierarchy of single- or multiple lineage precursors exhibiting various degrees of maturation arrest. The heterogeneity of AML is evident from the wide variety of clinical manifestations, response to therapy, phenotypic features, and molecular and cytogenetic alterations (53), (54), (55). In clinical practice, the accurate diagnosis of AML subtypes is essential for risk stratification and treatment planning. The World Health Organization (WHO) and French American British (FAB) classification systems are currently used to subtype AML (50), (51), (56). Although the WHO classification system relies heavily on cytogenetic findings, these data are often not available at the time of diagnosis and initiation of treatment. Furthermore, the most frequent cytogenetic feature, which is identified in over 40% of the patients with AML, is the lack of any chromosomal alterations (57), (58). In patients with cytogenetically normal AML, specific gene mutations have been associated with certain AML subtypes (59), (60).
Therefore there is a need not only for better markers to distinguish the various forms of AML, but more specific treatments for the various forms of AML.